ライフサイエンスコーパス: PARP cleavage

1 , generation of reactive oxygen species, and PARP cleavage.

2 AD, the pancaspase inhibitor, suppressed the PARP cleavage.

3 on of caspases, and IETD similarly prevented PARP cleavage.

4 activation of procaspase-9, procaspase-3 and PARP cleavage.

5 e coupled with increased Bax/Bcl-2 ratio and PARP cleavage.

6 ytochrome c release, caspase-3 activity, and PARP cleavage.

7 l lines resulted in apoptosis as measured by PARP cleavage.

8 ition of Ac-YVAD-cho to the cultures blocked PARP cleavage.

9 D437 did not induce caspase-3 activation and PARP cleavage.

10 l the activation of caspases as indicated by PARP cleavage.

11 k activity and markedly increased TG-induced PARP cleavage.

12 or cells; and activated caspase-3 leading to PARP cleavage.

13 is by DNA damage, resulting in caspase-3 and PARP cleavage.

14 methacrylate) stimulates TPT-induced PCD and PARP cleavage.

15 duced apoptosis, activation of SAPK/JNK, and PARP cleavage.

16 This cleavage occurs shortly after PARP cleavage.

17 stages of apoptosis in this system and after PARP cleavage.

18 nsferrin or FeCl(3) suppressed SubAB-induced PARP cleavage.

19 is-Asp(O-methyl)-fluoromethylketone prevents PARP cleavage.

20 sistant cells to AZD6244 by inducing BIM and PARP cleavage.

21 ble-strand breaks, caspase-8 activation, and PARP cleavage.

22 optosis were identified by TUNEL labeling or PARP cleavage.

23 from mitochondria, caspase-3 activation and PARP cleavage.

24 pontaneous and fludarabine-induced Mcl-1 and PARP cleavage.

25 stic induction of caspases-3, -8, and -9 and PARP cleavage.

26 totic phenotype as revealed by caspase-3 and PARP cleavage.

27 tion of caspase-3, caspase-8, caspase-9, and PARP cleavage.

28 was not accompanied by caspase activation or PARP cleavage.

29 xin-V/PI staining, caspase-3 activation, and PARP cleavage.

30 by pycnotic nuclei, annexin V staining, and PARP cleavage.

31 nfection led to a reduction in the amount of PARP cleavage.

32 ges in mitochondrial membrane potential, and PARP cleavage.

33 X suppressed ERK and p38 phosphorylation and PARP cleavage.

34 ase-8, caspase-9, and caspase-3, followed by PARP cleavage.

35 Annexin-V staining, caspase-3 activation and PARP cleavage.

36 t transactivation and induction of TRAIL and PARP cleavage.

37 ed with enhanced procaspase (3, 8 and 9) and PARP cleavage.

38 spase-3 activity, cleavage of caspase-3, and PARP cleavage.

39 optosis, cell surface Annexin V staining and PARP cleavage.

40 membrane potential, caspase activation, and PARP cleavage.

41 ctivation of terminal caspases, resulting in PARP-cleavage.

42 d poly (adenosine diphosphate [ADP]) ribose (PARP) cleavage.

43 substrates and poly (ADP ribose) polymerase (PARP) cleavage.

44 activation, and poly(ADP-ribose) polymerase (PARP) cleavage.

45 yadenosine-5'-diphosphate-ribose polymerase (PARP) cleavage.

46 laddering and poly (ADP-ribose) polymersae (PARP) cleavage.

47 of Fas- induced poly-ADP ribose polymerase (PARP) cleavage.

48 d detection of poly (ADP-ribose) polymerase (PARP) cleavage.

49 f caspases, and poly(ADP-ribose) polymerase (PARP) cleavage.

50 tress based on poly (ADP-ribose) polymerase (PARP) cleavage.

51 nied full-length poly ADP ribose polymerase (PARP) cleavage.

52 rmed by assay of poly ADP-ribose polymerase (PARP) cleavage.

53 as well as with poly(ADP)ribose polymerase (PARP) cleavage.

54 se activity and poly(ADP-ribose) polymerase (PARP) cleavage.

55 activation and poly-(ADP-ribose) polymerase (PARP) cleavage.

56 and (TRAIL) and poly(ADP-ribose) polymerase (PARP) cleavage.

57 and Dex induce poly (ADP ribose) polymerase (PARP) cleavage, a signature event of apoptosis.

58 hibitor blocked ATM phosphorylation, induced PARP cleavage, abrogated cell cycle checkpoint activatio

59 ce of dopamine-stimulated apoptosis included PARP cleavage, activation of mitochondrial-derived caspa

60 unoblotting for poly(ADP-ribose) polymerase [PARP] cleavage; activation of caspases-3, -8, and -9; ex

61 po B- or Apo-2L/TRAIL-induced processing and PARP cleavage activity of caspase-3.

62 greater cytosolic accumulation of cyt c and PARP cleavage activity of caspase-3.

63 Marked caspase-3-like PARP cleavage activity, proteolytic processing of CPP32

64 ted significant poly(ADP-ribose) polymerase (PARP) cleavage after exposure to Stx1 or Stx2.

65 ath receptor DR5 led to complete ablation of PARP cleavage and apoptosis, indicating the essential ro

66 avage of procaspase 3, 8, and 9 and enhances PARP cleavage and apoptosis.

67 siRNA) in C4-2 cells significantly prevented PARP cleavage and apoptosis.

68 RA synovial fibroblasts to TNFalpha-induced PARP cleavage and apoptotic cell death.

69 Furthermore, PARP cleavage and caspase activation were confined exclu

70 sed ratio of cells in the subG1 phase and by PARP cleavage and caspase activation.

71 lls also generated apoptosis as reflected by PARP cleavage and DNA fragmentation indicating a cell su

72 e of cytochrome c, caspase-3 activation with PARP cleavage and DNA fragmentation.

73 It blocks AB(1-42)-mediated PARP cleavage and increases the levels of anti-apoptotic

74 It blocks Abeta(1-42)-mediated PARP cleavage and increases the levels of anti-apoptotic

75 static human mammary tumor, was resistant to PARP cleavage and loss of viability in response to actin

76 formed cells, as evidenced by an increase in PARP cleavage and partial inhibition of this effect by t

77 ERK activity potentiated paclitaxel-induced PARP cleavage and phosphatidylserine externalization, su

78 ition of JNK, p38 MAPK, or MEK did not alter PARP cleavage and the cell death induced by paclitaxel.

79 fragmentation, poly (ADP-ribose) polymerase (PARP) cleavage and activation of caspase-3 and -8.

80 ed caspase-3 and poly(ADP)ribose polymerase (PARP) cleavage and apoptosis (>50% 2 micromol/L, 48 h).

81 nduce elevated poly (ADP-ribose) polymerase (PARP) cleavage and apoptosis.

82 ly(adenosine diphosphate-ribose) polymerase (PARP) cleavage and cleavage of caspase-3 substrates, sug

83 with increased poly(ADP-ribose) polymerase (PARP) cleavage and cytochrome c release was observed in

84 splayed elevated poly ADP-ribose polymerase (PARP) cleavage and susceptibility to camptothecin-induce

85 inhibition of cell growth, colony formation, PARP cleavage, and apoptosis.

86 injury, activation of procaspases-3 and -8, PARP cleavage, and apoptosis.

87 s, as indicated by histology, DNA laddering, PARP cleavage, and caspase-3 activation.

88 as evidenced by induction of DNA laddering, PARP cleavage, and caspase-3/9 activities.

89 G2 arrest, leading to caspase-3 activation, PARP cleavage, and cell apoptosis.

90 by increases in Annexin V binding activity, PARP cleavage, and chromatin disorganization.

91 marked effect on HB cell viability, induced PARP cleavage, and decreased CDK9 protein expression in

92 c, but it did prevent caspase-3 activation, PARP cleavage, and DNA fragmentation.

93 ase of cytochrome c, caspase activation with PARP cleavage, and DNA fragmentation.

94 rome c but did prevent caspase-3 activation, PARP cleavage, and DNA fragmentation.

95 r UV treatment, as measured by caspase-7 and PARP cleavage, and IGF-I co-treatment protected against

96 CH2F prevented caspase activation, inhibited PARP cleavage, and inhibited cell death.

97 uces apoptosis by activating caspase 3/7 and PARP cleavage, and its longer exposure causes increase i

98 fied which involved procaspase-7 activation, PARP cleavage, and nuclear condensation.

99 n caused significantly greater caspase-3 and PARP cleavage, and the combined toxicity also was inhibi

100 ced DNA fragmentation, cytochrome c release, PARP cleavage, and the formation of active caspase 3.

101 w pI) release), poly(ADP-ribose) polymerase (PARP) cleavage, and apoptosis.

102 denosine 5'-diphosphate]-ribose) polymerase (PARP) cleavage, and apoptotic cell death.

103 ochrome c (CC), poly(ADP-ribose) polymerase (PARP) cleavage, and DNA fragmentation.

104 on of caspase-3, poly(ADP-ribose)polymerase (PARP) cleavage, and DNA fragmentation.

105 h caspase-3 and poly(ADP-ribose) polymerase (PARP) cleavage, and inhibited constitutive activation of

106 procaspase-3 and poly(ADP-ribose)polymerase (PARP) cleavage, and reduced p53 and p21 levels.

107 ansferase dUTP nick-end labeling positivity, PARP cleavage, Annexin V positivity, and drug-induced ce

108 5 inhibited 2-ME-induced caspase activation, PARP cleavage, apoptosis and reversed mitochondrial memb

109 nt effects on Akt phosphorylation, caspase-3/PARP cleavage, apoptotic phenotype, and cell viability,

110 caspases activity increase and caspases and PARP cleavage as well as a lack in cytochrome c release

111 In contrast, zVAD-FMK blocked PARP cleavage as well as loss of delta psi(m) and cell d

112 sub-G(1) phase cells; caspase-3 and -9, and PARP cleavage as well as morphological signs of apoptosi

113 on and enhanced poly(ADP-ribose) polymerase (PARP) cleavage as a result of bortezomib, in the presenc

114 as found to induce nuclear fragmentation and PARP cleavage, as well as to arrest cells at the G(2)/M

115 signaling-p53 increase, AMPK activation, and PARP cleavage-as well as autophagy induction were also i

116 f oligomer induced apoptosis, according to a PARP-cleavage assay.

117 oly-adenosine diphosphate ribose polymerase (PARP) cleavage at low concentrations of EGCG (3 microg/m

118 In contrast, caspase inhibitors prevented PARP cleavage but not cytochrome c release, suggesting t

119 these events (e.g. caspase-3 activation and PARP cleavage) but did not block cytochrome c release or

120 Z-VAD-FMK inhibits PARP cleavage, but does not alter the AGN193198-dependen

121 The 24-kDa product of PARP cleavage by caspase-3 may contribute to the irrever

122 TM small-molecule inhibitors that attenuated PARP cleavage by inhibiting gamma-H2AX, which in turn in

123 The prevention of PARP cleavage by inhibition of caspase-3 resulted in a 1

124 deprivation for 4 h increased cell death and PARP cleavage by promoting activation of caspase-8 and c

125 , methotrexate) caused minimal caspase-3 and PARP cleavage by themselves, and their toxicity was not

126 se of measuring poly(ADP-ribose) polymerase (PARP) cleavage by Western blot, as an index of apoptosis

127 roteins, cdc6, MCM2, cdc25A, nor increase in PARP cleavage, caspase activation and the 30-300 kb DNA

128 1 and Gli2 expression and induced gammaH2AX, PARP cleavage, caspase-3 activation, and cell death.

129 ilization, cytochrome c release, caspase and PARP cleavage, consistent with the hypothesis that p38(M

130 Whereas PARP cleavage defined cell death in most other cell type

131 lls with zAPFcmk alone led to characteristic PARP cleavage, depletion of the precursor forms of two I

132 d apoptosis as demonstrated by caspase-3 and PARP cleavage, DNA fragmentation, and nuclear condensati

133 Asp-fluoromethylketone (Z-VAD-fmk) inhibited PARP cleavage, DNA fragmentation, calpain activation, an

134 ivation and Bax cleavage but did not inhibit PARP cleavage, DNA fragmentation, or 9-amino-20(S)-campt

135 tely prevented poly (ADP-ribose) polymerase (PARP) cleavage, E(2)-inhibited growth, and apoptotic mor

136 spase-3/CPP32 and caspase-7/Mch3 followed by PARP cleavage, effects that can be blocked either by SPP

137 poptosis as determined by DNA fragmentation, PARP cleavage, fluorescence microscopy and flow cytometr

138 PARP cleavage followed caspase activation and reached ma

139 trophy was also confirmed by the presence of PARP cleavage (H: 74+/-7 versus T: 41+/-4 arbitrary dens

140 optosis was determined by TUNEL staining and PARP cleavage (immunoblotting of nuclear extracts) and c

141 caspase-3 activation, and partially reduced PARP cleavage in a concentration-dependent manner.

142 The role of PARP cleavage in apoptosis has now been investigated in

143 targeted Bak leads to enhanced caspase 7 and PARP cleavage in comparison with the ER-targeted Bak.

144 in NOD mice, suppressed thapsigargin-induced PARP cleavage in human islets, and attenuated ERK1/2 and

145 viral MET RNA interference construct induces PARP cleavage in MM.1S cells.

146 ulation of sub-G(1) population and block the PARP cleavage in response to etoposide.

147 nM, and triggers activation of caspases and PARP cleavage in the MDA-MB-231 breast cancer cell line.

148 Patients having caspase-3 activation and PARP cleavage in vivo had a significantly lower blood le

149 caspase-3, and poly(ADP-ribose) polymerase (PARP) cleavage in blood leukemia cells immediately follo

150 Bid and protein poly(ADP-ribose) polymerase (PARP) cleavage in HeLa cells lacking MTS-hOGG1.

151 agmentation and poly(ADP-ribose) polymerase (PARP) cleavage in LA-treated MCF10A cells indicated prog

152 did not induce poly(ADP-ribose) polymerase (PARP) cleavage in virus-negative BJAB cells.

153 ulation of MAP and p70S6K growth kinases and PARP cleavage; in contrast, IL-6 does not inhibit IR-ind

154 agy, and robust poly(ADP-ribose) polymerase (PARP) cleavage indicative of DNA damage and apoptosis.

155 JNK activation and PARP cleavage induced by 30 nM Taxotere at 48 h were rev

156 elation between both assays, indicating that PARP cleavage is an accurate method to examine PCD.

157 B3(Fv)-PE38-induced PARP cleavage is inhibited by several protease inhibitor

158 after nsPEF and poly-ADP ribose polymerase (PARP) cleavage is detected in 2 hr.

159 CPV gave no PARP-cleaving activity, and all PARP cleavage mediated by SPI-2 and CrmA mutants of RPV

160 These data demonstrate that PARP cleavage occurs during glucocorticoid-induced apopt

161 that LtxA causes activation of caspases and PARP, cleavage of pannexin-1 (Panx1) channels, and expul

162 Like PARP, cleavage of these substrates in apoptotic cell ext

163 t-A significantly induces the cell death and PARP-cleavage of both CSC and non-CSC cells.

164 Bax cleavage and calpain activation, but not PARP cleavage or cell death.

165 ng and lysis of DHL-4 cells, without caspase/PARP cleavage or TUNEL-positivity, suggesting a necrotic

166 Conversely, propidium iodide staining, PARP cleavage patterns, and random DNA fragmentation rev

167 with increased poly(ADP-ribose) polymerase (PARP) cleavage, phosphatidylserine externalization, and

168 ated prior to the detection of caspase 3 and PARP cleavage, primary indicators of cell death, whereas

169 nstrated by an obvious increase of the 89-kD PARP cleavage product, which was observed at almost the

170 the presence of a cathepsin-associated 55 kD PARP cleavage product.

171 and cyclin D1, whereas caspase activity and PARP cleavage products were increased in tumors of drug-

172 id not recognize the Mr approximately 90,000 PARP cleavage products, in contrast to the parent enzyme

173 h DEVD inhibited the chromatin condensation, PARP cleavage, release of apoptotic bodies, and release

174 creased and prolonged caspase 3 activity and PARP cleavage, suggesting that the sensitization to TRAI

175 anoikis involved caspase-3- and -7-mediated PARP cleavage that was initiated by caspase-8 and probab

176 apoptosis in both glioma cells by promoting PARP cleavage, triggering DNA damage, and increasing ROS

177 pase-8, caspase-9, and caspase-3 activation, PARP cleavage, upregulation of Fas-L, Fas, FADD and DR4,

178 Reduced PARP cleavage was also observed in cells treated with tu

179 PARP cleavage was not delayed in XPD LCLs in response to

180 st, a slight, but significant enhancement of PARP cleavage was observed in dephosphorylated extracts,

181 The timing and intensity of PARP cleavage was similar to that of JNK activation.

182 poly(ADP-ribose) polymerase (PARP) cleavage was noted in all Kit mutant lines after i

183 into the cytosol, caspase 3 activation, and PARP cleavage were also detected in these cells.

184 Activation of multiple caspases and PARP cleavage were also observed in the C4-2 tumors trea

185 thamphetamine-induced caspase-3 activity and PARP cleavage were also reduced in c-Jun heterozygous kn

186 induced apoptosis, caspase-8 activation, and PARP cleavage were inhibited by knocking down DR5 using

187 Furthermore, DNA ladder formation and PARP cleavage were observed after treatment for 24 h, in

188 DNA ladder formation, CPP32 activation, and PARP cleavage were observed after treatment with geniste

189 s, in which increased caspase-3 activity and PARP cleavage were observed, but not in PC-3 cells, in w

190 ivity as well as poly-ADP ribose polymerase (PARP) cleavage were increased.

191 the induction of poly-ADP-ribose polymerase (PARP) cleavage were more pronounced and evident 12 h ear

192 er formation and poly-ADP ribose polymerase (PARP) cleavage were performed to measure the induction o

193 , decrease of Bax expression and increase of PARP cleavage) were blocked by the purinergic P2X(7) rec

194 ese drugs also did not increase caspase-3 or PARP cleavage when combined with TRAIL.

195 sub-G(0)/G(1) phase, caspase activation, and PARP cleavage), whereas cells harboring wild-type (wt)-F

196 r with AZD6244 induced expression of BIM and PARP cleavage, whereas activation of the STAT3 pathway i

197 lketone, inhibited PDT-induced apoptosis and PARP cleavage, whereas the inactive peptide analogue, be

198 shock induces poly (ADP-ribose) polymerase (PARP) cleavage, which triggers cellular toxicity.

199 1 h and induced activation of caspase 3 and PARP cleavage within 24 h.